{"id":739931,"date":"2026-07-03T00:38:17","date_gmt":"2026-07-03T00:38:17","guid":{"rendered":"https:\/\/www.newsbeep.com\/us\/739931\/"},"modified":"2026-07-03T00:38:17","modified_gmt":"2026-07-03T00:38:17","slug":"the-top-10-misleading-claims-about-antidepressants","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/us\/739931\/","title":{"rendered":"The Top 10 Misleading Claims About Antidepressants"},"content":{"rendered":"\n

In the past year, American psychiatry has been in the spotlight\u2014though perhaps \u201cin the hot seat\u201d would be a more fitting metaphor. The safety and efficacy of psychiatric medications\u2014particularly antidepressants\u2014has been questioned<\/a> at the highest levels of the US Department of Health and Human Services.1 Sensational claims of harm stemming from the use of antidepressants have filtered into the popular press, and medically-unsupervised lay groups claiming to provide safe methods of tapering antidepressants have been increasingly active. Though quite understandable, given longstanding controversies surrounding psychiatric medications, these developments should concern all psychiatrists.<\/p>\n

In this commentary, we examine 10 misleading claims about antidepressants. To be clear: most psychiatrists will recognize varying degrees of truth in several of these assertions, and we need to remain open to legitimate concerns about antidepressants. However, we view all 10 claims as misleading or simplistic at best. Here is why:<\/p>\n

1. All antidepressants are alike, with essentially the same risks and adverse effects.<\/p>\n

Criticism of antidepressants, especially in the popular media, typically groups all antidepressants together. Alternatively, many critiques focus on what are misleadingly called \u201cSSRIs\u201d, even though several agents in this class are not entirely selective for inhibition of serotonin reuptake. For example, sertraline has dopaminergic effects, while paroxetine has noradrenergic and anticholinergic effects.2 Perhaps most notably, the noradrenergic\/dopaminergic antidepressant bupropion is rarely discussed, despite the fact that it has very few of the side effects associated with serotonergic agents, such as sexual dysfunction or emotional blunting. Indeed, bupropion and vortioxetine may actually counter-act emotional blunting.3,4<\/p>\n

2. Antidepressants work by numbing emotions.<\/p>\n

Some critics have claimed that antidepressants work by \u201cnumbing emotions.\u201d5 It is true that decreased emotional responsiveness can occur in a substantial proportion of patients taking serotonergic agents. This is distressing to patients and is associated with poor adherence to treatment; however, there is no credible evidence that emotional blunting is the active mechanism underlying antidepressant effects. On the contrary: based on use of the gold standard measure of emotional blunting\u2014the Oxford Depression Questionnaire\u2014it is clear that successful antidepressant treatment is correlated with reduced levels of emotional numbing during the course of treatment.6 Furthermore, agents with minimal risk of emotional blunting, such as bupropion and vortioxetine, are demonstrably effective antidepressants.4<\/p>\n

3. Antidepressants are just expensive placebos or \u201csugar pills.\u201d<\/p>\n

Few mood disorder specialists would argue that currently available antidepressants are robustly effective for all patients. Equally few specialists would endorse the common claim in the popular press that, \u201cAntidepressants work no better than no treatment at all;\u201d or that, \u201cantidepressants are no better than a sugar pill.\u201d As a comprehensive review observed, \u201cThis conclusion represents an incorrect interpretation of the data, which may have the dangerous public health consequence of dissuading patients with depression from accessing treatment.\u201d7<\/p>\n

Notably, in a meta-analysis by Cipriani et al, reviewing 522 trials representing over 116,000 patients, the study showed that all 21 antidepressants studied outperformed placebos. However, the standard mean difference (SMD) of 0.30 was small, and corresponds to a modest 2-point reduction on the 17-item Hamilton Depression Rating Scale (HAM-D17).8 Understandably, the clinical significance of this small reduction has been challenged.9<\/p>\n

To be clear: it is widely recognized that the nonspecific (nonpharmacologic) effect of antidepressants is very large, accounting for at least two-thirds of the response to the medication, and in some studies, more than 80%.10 Rutherford and Roose observed that, \u201cin antidepressant trials for adults, placebo response averages 31% compared with a mean medication response of 50%…\u201d7 In essence, this means that the active pharmacologic effect gets an extra 19% of the patient population better than would be the case with placebo. Similarly, Stone et al, examining individual participant data, estimated that about 15% of the patient population experienced a large, clinically significant response specifically attributable to the active drug.11 Both studies highlight that while the overall response to medication is high, the specific pharmacological benefit applies to a distinct minority of the treatment group.<\/p>\n

However, if we apply the 15% to 19% specific drug benefit figure to the US population receiving antidepressant treatment\u2014roughly 45 million individuals\u2014it means that about 6.75-8.55 million individuals are experiencing a large, potentially life-altering reduction in depressive symptoms (an average 16-point drop on the HAM-D). This is by no means a trivial outcome from the public health perspective. It is also important to note that for severe or melancholic major depressive disorder<\/a> (MDD), the placebo response drops significantly, and the specific chemical effect of the antidepressant becomes distinct and clinically meaningful.12<\/p>\n

Notably, the Stone et al study relied on the 17-item Hamilton Rating Scale for Depression (HAMD-17) as its standard metric. When a version of the Hamilton Depression Scale is used that evaluates core depressive symptoms (the HAM-D6), the drug-placebo difference rises from a modest approximate 0.30 on the HAM-D17 up to a clinically meaningful approximate 0.40 or higher on the HAM-D6.13 Furthermore, the Stone et al study involved acute antidepressant monotherapy. In clinical practice, psychiatrists \u201ctreat to remission,\u201d often using augmentation strategies and multiple antidepressant trials.<\/p>\n

Importantly, clinical trials and meta-analyses show that antidepressants consistently perform better than placebos at preventing depressive relapse (ie, symptoms returning within 6 months of remission). For example, Sim et al found that in 45 reports of 72 trials (n = 14, 450 subjects) lasting 33.4 weeks, antidepressants were more effective than placebos in preventing relapses (response rates [RR] = 1.90, confidence interval [CI]: 1.73\u20132.08; NNT = 4.4; P < 0.0001).14 Indeed, the UK’s National Institute for Health and Care Excellence guidelines (2022) note that for patients at high risk of relapse (eg, those with multiple prior episodes of MDD), maintenance antidepressant treatment for up to 2 years may cut the risk of relapse in half.15 That said, the issue of preventing recurrence\u2014or symptoms returning after a patient has been in remission for 6 months or longer\u2014is more complicated and controversial, as discussed here under long-term treatment.<\/p>\n

Finally, it is worth noting that placebo studies do not merely hand subjects an inert pill and push them out the door. In a standard phase 3 antidepressant trial, patients with depression in the placebo group are provided as many as 8 to 12 hours of personal contact and support with professional staff. As Rutherford and Roose note, \u201c\u2026being assigned to placebo in an antidepressant trial is far from \u201cno treatment,\u201d since it entails intensive contact with health care staff that greatly exceeds what is delivered in standard community treatment.\u201d7<\/p>\n

4. Antidepressants are addictive.<\/p>\n

Despite a widely-publicized statement likening antidepressants to heroin,16 there is no credible evidence that antidepressant use shows the key features of genuine addiction<\/a> (eg, drug craving, loss of control of drug intake, spending excessive time getting and using drug, neglecting personal responsibilities, and giving up social activities because of drug misuse). Indeed, SSRIs score no higher than a placebo on standard human abuse potential\u2014or \u201cdrug liking\u201d\u2014scales.17<\/p>\n

Furthermore, there is no conclusive evidence showing that the pathophysiological mechanisms underlying SSRI\/SNRI withdrawal symptoms are similar to those in alcohol, opioid<\/a>, barbiturate, or benzodiazepine withdrawal.18 One recent review concluded, \u201cThere is minimal evidence, using established classification systems and concepts, that antidepressants should be classified as addictive substances.\u201d19<\/p>\n

Although it is often claimed that tolerance develops to long-term use of antidepressants, this is not consistent with the most stringent definition of tolerance (ie, requiring higher and higher doses of a drug to achieve the same clinical effect). Unlike with genuine substances of abuse, such as alcohol or barbiturates, true tolerance is not commonly observed with antidepressants. The related phenomenon of tachyphylaxis\u2014defined as loss of a previously effective antidepressant treatment response despite staying on the same drug and dosage\u2014is observed in about 25% of patients with unipolar depression.20 Results from a study by Zimmerman et al show that the great majority of relapses attributed to so-called \u201cpoop out\u201d of the antidepressant are actually due to the initial response having been a placebo response.21 However, in our experience, the most common factor in loss of antidepressant response is poor adherence to the prescribed regimen (ie, simply not taking the medication).<\/p>\n

5. Antidepressants cause or provoke suicide.<\/p>\n

This literature is muddied by use of the ambiguous term suicidality, which conflates suicidal ideation with suicidal behavior. With respect to the well-known \u201cblack box\u201d warning on all antidepressant medications, highlighting an increased risk of suicidal thoughts and behaviors in children, adolescents, and young adults (up to age 24), there is credible evidence that the warning may actually have backfired by reducing necessary prescriptions and possibly increasing suicide attempts in this age group.22<\/p>\n

Furthermore, there is no credible evidence that antidepressants increase completed suicide or suicide attempts in older populations. In fact, the very same \u201cblack box\u201d warning notes that antidepressants are associated with a reduction in suicidality (suicidal thinking and behavior) in adults aged 65 and older, compared with a placebo.23 In addition, epidemiological studies do not support a link between antidepressant prescription and suicide rates<\/a>. Indeed, macro-level prescription data reveal that increases in prescriptions for SSRIs and other new-generation non-SSRIs are associated with lower suicide rates, based on US county-level suicide rate data.24<\/p>\n

6. Antidepressants provoke violence and mass shootings.<\/p>\n

Careful reviews have concluded that there is no established causal link between antidepressant use and mass violence, including school shootings.25 Thus, Knoll and Pies concluded<\/a> that \u201c\u2026The preponderance of recent research does not point to a link between antidepressants and mass shootings; ie, there is little or no evidence showing that perpetrators of mass shootings are more likely than those in the general public to have used, or to have been prescribed, antidepressants prior to the shooting.\u201d25<\/p>\n

Similarly, Hall et al concluded, \u201c\u2026it appears that most school shooters were not previously treated with psychotropic medications \u2013 and even when they were, no direct or causal association was found linking medication treatment to the crime.\u201d26 Given that a subset of school shooters with nonspecific emotional disturbances may receive psychiatric medications,25 confounding bias may lead to the unwarranted conclusion that the medication caused the shooter\u2019s behavior.<\/p>\n

7. Antidepressants are vastly overprescribed.<\/p>\n

This widely-held claim oversimplifies a complex pattern of antidepressant prescription in the US, in which differences in study methods and health care systems may lead to differences in frequency and duration of prescribing. To be sure: antidepressant use and prescribing have increased significantly in the past 30 years. Most of this increase is due to prescribing by primary care providers, not psychiatrists, and reflects a growing pool of patients kept on antidepressants for prolonged periods.27<\/p>\n

Such increased use has raised concerns about overprescribing for patients with less severe depression, and those who may not need medication for the long-term. Some evidence from cross-sectional community surveys supports this concern; In the 2010 National Survey on Drug Use and Health, only 44% of respondents using antidepressants reported experiencing a major depressive episode during the past year.28 However, as Simon et al point out, \u201cCross-sectional community surveys\u2026may not accurately assess indications for antidepressant treatment\u2026[because] more remote episodes of depression are often under-reported.\u201d In their own study of outpatients in four large health care systems, Simon et al found that \u201c\u2026prescribing of antidepressant medication for minimal or mild depression is much less common than suggested by previous reports,\u201d amounting to no more than 18% of patients. The authors concluded that, \u201c\u2026overprescribing of antidepressants for mild depression is not a significant public health concern.\u201d29<\/p>\n

Furthermore, Thornicroft et al found that only a small minority of participants with MDD received minimally adequate treatment (pharmacotherapy or psychotherapy<\/a>), amounting to 1 in 5 people in high-income and 1 in 27 in low-\/lower-middle-income countries.30 And while as many as 1 in 6 Americans are taking an antidepressant, a large proportion are likely undertreated, as they do not meet criteria for minimally adequate treatment. For example, in a multi-site, NIMH sponsored study, only 33% of the 801 subjects enrolled had ever had a prior adequate trial of antidepressant medication.31 An earlier study by Keller et al found adequate antidepressant trials in only 27% of patients with chronic depression.32<\/p>\n

There is also evidence of underprescribing in some minority populations. For example, among individuals with PHQ-9 scores \u226510, indicating moderate to severe depressive symptoms, only 13% to 15% of Black and Asian American respondents were currently receiving antidepressants, compared with 27.3% of White respondents.33 Similarly, in a study of veterans, among patients with severe depression for whom antidepressant treatment is clinically indicated, White patients were 1.87 times more likely than Black patients to receive an antidepressant prescription.34<\/p>\n

Furthermore, a large body of evidence shows that depression is underrecognized and undertreated in geriatric patient samples, often with inadequate dosing of antidepressants. Low rates of adequate depression care in older persons with chronic illnesses have also been reported.35<\/p>\n

Finally, it is notable that the vast majority of US adults with depression receive no psychiatric treatment at all. Specifically, only 28.7% of adults who screened positive for active depression received any psychiatric treatment (either medication or psychotherapy) during the survey year.36<\/p>\n

In sum: the notion that antidepressants are vastly overprescribed in the US is, at best, an oversimplification of a complex issue.<\/p>\n

8. Antidepressants mask the \u201croot causes\u201d of depression and interfere with psychotherapy.<\/p>\n

This is a popular trope among many critical psychiatry groups. The claim assumes that we can reliably determine the root causes of depression for any given patient; whereas in fact, clinically significant depression is often determined by a myriad of biopsychosocial causes. As a recent comprehensive review concluded, the determinants of depression include, \u201c\u2026the microbiome, dysregulation of the HPA axis, inflammatory reactions, the kynurenine pathway, as well as psychological and social factors. It may be that physical factors are proximal determinants of depression, which, in turn, are acted on by more distal social factors, such as deprivation, environmental events, and social capital.\u201d37<\/p>\n

Furthermore, there is no credible evidence that antidepressants interfere with a psychodynamic understanding of depression, or that combining medication with psychotherapy interferes with the latter. On the contrary, several studies find the combination superior to either treatment alone for moderate-to-severe MDD.38 As David Mintz, MD, has pointed out38: \u201cCombined treatment produces not only faster and greater short-term benefits, but greater long-term benefits as well\u2026The 2 modalities may exert an additive effect by addressing different symptom domains. Therapy, for example, might address the hopelessness related to depression, while medications more directly address neurovegetative aspects of depression.\u201d<\/p>\n

9. Antidepressants frequently provoke serious, prolonged withdrawal syndromes.<\/p>\n

Unfortunately, we lack controlled studies of the frequency, severity, and duration of antidepressant withdrawal symptoms, using both (1) the standardized assessment tool, the Discontinuation-emergent Signs and Symptoms checklist (DESS); and (2) long tapering periods (> 2months). The best available data do not support the claim that withdrawal reactions are usually serious or very prolonged (>2 months). However, a small minority of patients do experience severe and prolonged withdrawal symptoms, which can be very distressing. Much depends on the specific antidepressant, the dose, the tapering period, and possibly the duration of drug exposure.39<\/p>\n

While it is difficult to find a well-validated average duration of withdrawal symptoms, a systematic review by Fava et al (2018) concluded that \u201c\u2026symptoms typically ensued within a few days from discontinuation and lasted a few weeks\u2026\u201d; however, \u201c\u2026late onset and\/or a longer persistence of disturbances occurred as well.\u201d40<\/p>\n

A 2019 study by Henssler et al evaluated 40 controlled trials, 38 cohort studies, and 271 case reports of withdrawal. The review concluded that \u201cWithdrawal manifestations are usually mild and self-limiting; common ones include dizziness, headache, sleep disturbances, and mood swings. More serious or prolonged manifestations rarely arise\u2026 Controlled, high-quality studies point to a primarily self-limiting course involving mild symptoms. In rare cases, symptoms that were classified as more severe were seen.\u201d41<\/p>\n

These findings are in contrast to uncontrolled studies and online surveys, which suggest much higher incidence rates of antidepressant withdrawal effects in general, as well as more severe symptoms.42<\/p>\n

Subsequently, Henssler et al performed the first meta-analytic assessment of the incidence of antidepressant discontinuation symptoms and of placebo effects. Their study found that\u2014considering nonspecific (\u201cnocebo\u201d) effects\u2014the incidence of antidepressant discontinuation symptoms was approximately 15%, affecting about 1 in 6 to 7 patients who discontinue their medication. About 1 in 35 patients (roughly 3%) were found to have severe antidepressant discontinuation symptoms. Antidepressant agents differed substantially in the risk of inducing withdrawal symptoms. Within the selective serotonin reuptake inhibitor\/selective serotonin-norepinephrine reuptake inhibitor group, discontinuation symptoms were most frequently observed and most severe with desvenlafaxine, venlafaxine, and paroxetine.43<\/p>\n

Clinical experience suggests that discontinuation after very long antidepressant exposure (> 2 years) increases the risk of serious withdrawal reactions, though this has not been borne out in several meta-analyses.43 Similarly, clinical experience almost uniformly suggests that a very gradual taper (eg, over 2-4 months) achieves better outcomes than a very rapid taper, though results from one recent study did not confirm this.44 This puzzling discrepancy may be due to the lack of studies using tapering period exceeding 2 months (which we generally recommend).<\/p>\n

Some patients who have great difficulty discontinuing the antidepressant may require hyperbolic tapering,as described by Horowitz and Taylor.45 Others may benefit from use of the long-acting agent, fluoxetine, as a bridge to complete the discontinuation of a shorter-acting agent.46 A recent publication by the American Society of Clinical Psychopharmacology has provided guiding principles<\/a> regarding how and when antidepressant discontinuation should be considered.47<\/p>\n

In sum: while we lack definitive, controlled studies, clinical experience suggests that (1) serious and\/or prolonged withdrawal reactions are relatively uncommon, (2) withdrawal symptoms typically last a few weeks, and (3) serious withdrawal symptoms can usually be avoided with slow drug tapering of the medication over 2 to 4 months, avoidance of short-acting agents, and careful monitoring of the patient\u2019s comfort level.39<\/p>\n

10. Antidepressants are not effective, long-term, for preventing recurrence.<\/p>\n

This remains an area of uncertainty, since, for many antidepressants, we have limited evidence for long term recurrence prevention beyond 2 years, based on randomized controlled trials. This has led some critics to infer, fallaciously, that antidepressants are not clinically useful or effective, past the acute phase of treatment. Not surprisingly, the situation is more complicated. Indeed, there is ongoing debate as to how maintenance and recurrence prevention studies should be conducted and whether they should use an enriched design. Some have argued that the latter tends to skew the results in favor of the active drug.48 And while it is clear that antidepressants prevent depressive relapse, it is more difficult to demonstrate a true prophylactic effect, or the prevention of actual recurrence of depressive episodes after a patient has been in remission for 6 months or longer.<\/p>\n

For example, a review by El-Mallakh and Briscoe found that, \u201cAfter treatment of an acute depressive episode, antidepressants clearly prevent relapse back into the same depressive episode. This is demonstrated by an adequate number of randomized, blinded, placebo-controlled, 1-year continuation trials. The ability of antidepressants to prevent recurrence of future episodes is less clear. Randomized, blinded, placebo-controlled trials of 18 months or longer are infrequent – 18 studies were identified. While nearly all show that antidepressant continuation is superior to placebo in preventing resurgence of depressive symptoms, nearly all of the difference occurs in the first 6 months after randomization.\u201d49 The authors concluded that, \u201cThese findings may challenge the hypothesis that antidepressants provide prophylaxis against depressive episodes.\u201d<\/p>\n

To be sure, the PREVENT study of venlafaxine extended release found that, by the end of 2 years, the cumulative probability of recurrence was 28.5% for the venlafaxine ER group and 47.3% for the placebo group.50 However, this study used an enriched randomized, discontinuation design, in which only patients who have already demonstrated a positive response and good tolerability to the drug during the initial open or active treatment phase were randomized into the subsequent maintenance phase.<\/p>\n

Similarly, Sim et al showed that, in 35 reports of 37 trials (n = 7253) lasting 27.0 months, antidepressants were effective in preventing recurrences (RR = 2.03, CI 1.80-2.28; NNT = 3.8; P < 0.0001), with minor differences among drug types.14 Here, too, many of the studies used an enriched design, and the authors notably commented, \u201cSuch case selection is likely to limit potential generalization of findings to broader clinical populations.\u201d That said, the absence of high-quality, non-enriched studies showing genuine prophylaxis against recurrence does not demonstrate that long-term antidepressant treatment is inherently ineffective.<\/p>\n

Note that in the Sim et al study,14 the number needed to treat (NNT) of 3.8 is actually lower than that for acute antidepressant treatment (4.4). This might suggest that antidepressants are better at preventing recurrence than at achieving acute remission. However, the finding most likely reflects the gradual deterioration within the placebo group. Put another way: placebos eventually \u201cpeter out\u201d in the long-term treatment of depression, in contrast to active drug. Nevertheless, the Sim et al study provides evidence\u2014imperfect though it is\u2014that antidepressants can prevent recurrence for a period exceeding 2 years.<\/p>\n

In our experience, for many patients with 3 or more episodes of serious major depression, long-term antidepressant maintenance (2 years or longer) clearly helps prevent depressive relapse, and may also prevent recurrence after 6 months. This is consistent with the 2023 Canadian Network for Mood and Anxiety Treatments (CANMAT) report, which noted that \u201c\u2026In recent, large-sample RCTs examining maintaining or discontinuing antidepressants in stably treated patients, medication maintenance was associated with lower rates of recurrence during 1-year and 3-year follow-up.\u201d51 We also concur with the CANMAT recommendations that, \u201c\u2026For patients with risk factors for recurrence, antidepressant treatment should be continued for 2 years or more.\u201d That said, we acknowledge the pressing need for more randomized, blinded, placebo-controlled trials of 2 years or longer.<\/p>\n

Concluding Thoughts<\/p>\n

Currently available antidepressants are far from ideal medications, and SSRI\/SNRIs carry a substantial adverse effect burden. However, exaggerated claims of harm from antidepressants have unduly alarmed and misinformed the general public. This threatens the health and well-being of the substantial subset of patients who significantly benefit from antidepressant treatment. In our experience, with conservative prescribing; avoidance of short half-life agents; diligent monitoring; and careful attention to the discontinuation process, antidepressant treatment is generally safe, effective, and often life-enhancing for many patients with serious depression. Of course, medication is merely a bridge between feeling depressed and feeling better. The patient must still walk across that bridge and therein lies the role of self-exploration in psychotherapy. Indeed, in mild-to-moderate cases of MDD, we would recommend talk therapy as the treatment of first choice.<\/p>\n

Dr McIntyre\u00a0is a professor of psychiatry and pharmacology at the University of Toronto and head of the Mood Disorders Psychopharmacology Unit at the University Health Network in Toronto, Canada. He is also the executive director of the Brain and Cognition Discovery Foundation and director and cochair of the scientific advisory board of the Depression and Bipolar Support Alliance. He is a professor and Nanshan Scholar at Guangzhou Medical University in China, an adjunct professor at Korea University College of Medicine in Seoul, a clinical professor at the State University of New York Upstate Medical University in Syracuse, and a clinical professor in the Department of Psychiatry and Neurosciences at the University of California Riverside School of Medicine. He is the founder of the Canadian Rapid Treatment Centre of Excellence and CEO of Braxia Scientific Corp.<\/p>\n

Dr Pies\u00a0is professor emeritus of psychiatry and a lecturer on bioethics and humanities at SUNY Upstate Medical University in Syracuse, New York; a clinical professor emeritus of psychiatry at Tufts University School of Medicine in Boston, Massachusetts; and editor in chief emeritus of\u00a0Psychiatric Times\u00a0(2007-2010). Dr Pies is the author of several books, including several textbooks on psychopharmacology. A collection of his works can be found on\u00a0Amazon<\/a>.<\/p>\n

References<\/p>\n

1. HHS launches MAHA action plan to curb psychiatric overprescribing. US Department of Health and Human Services. May 4, 2026. Accessed June 30, 2026. https:\/\/www.hhs.gov\/press-room\/hhs-launches-maha-action-plan-curb-psychiatric-overprescribing.html<\/a><\/p>\n

2. Tatsumi M, Groshan K, Blakely RD, Richelson E. Pharmacological profile of antidepressants and related compounds at human monoamine transporters.<\/a> Eur J Pharmacol. 1997;340(2-3):249-258.<\/p>\n

3. Stahl SM, Pradko JF, Haight BR, et al. A review of the neuropharmacology of bupropion, a dual norepinephrine and dopamine reuptake inhibitor.<\/a> Prim Care Companion J Clin Psychiatry. 2004;6(4):159-166.<\/p>\n

4. Christensen MC, Adair M, Loft H, McIntyre RS. The Motivation and Energy Inventory (MEI): analysis of the clinically relevant response threshold in patients with major depressive disorder and emotional blunting using data from the COMPLETE study.<\/a> J Affect Disord. 2023;323:547-553.<\/p>\n

5. Moncrieff J. Against the stream: antidepressants are not antidepressants \u2013 an alternative approach to drug action and implications for the use of antidepressants.<\/a> BJPsych Bull. 2018;42(1):42-44.<\/p>\n

6. Dawson G, Pies RW. Antidepressants do not work by numbing emotions. Psychiatric Times. September 26, 2022. https:\/\/www.psychiatrictimes.com\/view\/antidepressants-do-not-work-by-numbing-emotions<\/a><\/p>\n

7. Rutherford BR, Roose SP. A model of placebo response in antidepressant clinical trials.<\/a> Am J Psychiatry. 2013;70(7):723-733.<\/p>\n

8. Cipriani A, Furukawa TA, Salanti G, et al. Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis.<\/a> Focus (Am Psychiatr Publ). 2018;16(4):420-429.<\/p>\n

9. Hengartner MP, Pl\u00f6derl M. Statistically significant antidepressant-placebo differences on subjective symptom-rating scales do not prove that the drugs work: effect size and method bias matter!<\/a> Front Psychiatry. 2018;9:517.<\/p>\n

10. Kirsch I. Antidepressants and the placebo effect.<\/a> Z Psychol. 2014;222(3):128-134.<\/p>\n

11. Stone MB, Yaseen ZS, Miller BJ, et al. Response to acute monotherapy for major depressive disorder in randomized, placebo-controlled trials submitted to the US Food and Drug Administration: individual participant data analysis.<\/a> BMJ. 2022;378:e067606.<\/p>\n

12. Brown WA. Melancholic\/endogenous depression and response to somatic treatment and placebo.<\/a> Am J Psychiatry. 1992;149(10):1324-1334.<\/p>\n

13. Bech P. The responsiveness of the different versions of the Hamilton Depression Scale.<\/a> World Psychiatry. 2015;14(3):309-310.<\/p>\n

14. Sim K, Lau WK, Sim J, et al. Prevention of relapse and recurrence in adults with major depressive disorder: systematic review and meta-analyses of controlled trials.<\/a> Int J Neuropsychopharmacol. 2015;19(2):pyv076.<\/p>\n

15. Depression in adults: treatment and management. National Institute for Health and Care Excellence. June 29, 2022. Accessed June 2, 2026. https:\/\/www.nice.org.uk\/guidance\/ng222\/chapter\/Recommendations<\/a><\/p>\n

16. Mole B. RFK Jr. plans to curb antidepressants which he falsely compares to heroin. Ars Tehnca. May 5, 2026. Accessed June 2, 2026. https:\/\/arstechnica.com\/health\/2026\/05\/rfk-jr-plans-to-curb-antidepressants-which-he-falsely-compares-to-heroin\/<\/a><\/p>\n

17. Zawertailo LA, Busto U, Kaplan HL, Sellers EM. Comparative abuse liability of sertraline, alprazolam, and dextroamphetamine in humans.<\/a> J Clin Psychopharmacology. 1995;15(2):117-124.<\/p>\n

18. Pies RW, Osser DN. Sorting out the antidepressant \u201cwithdrawal\u201d controversy.<\/a> Psychiatric Times. 2019;36(3).<\/p>\n

19. Jauhar S, Hayes J, Sharp T, Baldwin DS. Antidepressants, withdrawal, and addiction; where are we now?<\/a> J Psychopharmacol. 2019;33(6):655-659.<\/p>\n

20. Targum SD. Identification and treatment of antidepressant tachyphylaxis.<\/a> Innov Clin Neurosci. 2014;11(3-4):24-28.<\/p>\n

21. Zimmerman M, Thongy T. How often do SSRIs and other new-generation antidepressants lose their effect during continuation treatment? Evidence suggesting the rate of true tachyphylaxis during continuation treatment is low.<\/a> J Clin Psychiatry. 2007;68(8):1271-1276.<\/p>\n

22. Soumarai SB, Koppel R, Naci H, et al. Intended and unintended outcomes after fda pediatric antidepressant warnings: a systematic review.<\/a> Health Affairs. 2024;43(10)1360-1369.<\/p>\n

23. Stone M, Laughren T, Jones ML, et al. Risk of suicidality in clinical trials of antidepressants in adults: analysis of proprietary data submitted to US Food and Drug Administration.<\/a> BMJ. 2009;339:b2880.<\/p>\n

24. Gibbons RD, Hur K, Bhaumik DK, Mann JJ. The relationship between antidepressant medication use and rate of suicide.<\/a> Arch Gen Psychiatry. 2005;62(2):165-172.<\/p>\n

25. Knoll JL, Pies RW. No, antidepressants do not provoke mass shootings. Psychiatric Times. September 12, 2025. https:\/\/www.psychiatrictimes.com\/view\/no-antidepressants-do-not-provoke-mass-shootings<\/a><\/p>\n

26. Hall RCW, Friedman SH, Sorrentino R, et al. The myth of school shooters and psychotropic medications.<\/a> Behav Sci Law. 2019;37(5):540-558.<\/p>\n

27. Mojtabai R, Olfson M. National trends in long-term use of antidepressant medications: results from the U.S. National Health and Nutrition Examination Survey.<\/a> J Clin Psychiatry. 2014;75(2):169-77.<\/p>\n

28. Mojtabai R. Clinician-identified depression in community settings: concordance with structured-interview diagnoses.<\/a> Psychother Psychosom. 2013;82(3):161-169.<\/p>\n

29. Simon GE, Rossom RC, Beck A, et al. Antidepressants are not overprescribed for mild depression.<\/a> J Clin Psychiatry. 2015;76(12):1627-1632.<\/p>\n

30. Thornicroft G, Chatterji S, Evans-Lacko S, et al. Undertreatment of people with major depressive disorder in 21 countries.<\/a> Br J Psychiatry. 2017;210(2):119-124.<\/p>\n

31. Kocsis JH, Gelenberg AJ, Rothbaum B, et al. Chronic forms of major depression are still undertreated in the 21st century: systematic assessment of 801 patients presenting for treatment.<\/a> J Affect Disord. 2008;110(1-2):55-61.<\/p>\n

32. Keller MB, Harrison W, Fawcett JA, et al. Treatment of chronic depression with sertraline or imipramine: preliminary blinded response rates and high rates of undertreatment in the community.<\/a> Psychopharmacol Bull. 1995;31(2):205-212.<\/p>\n

33. Perlis RH, Ramachandiran AK, Verhaak PF, et al. Antidepressant use among American adults in a 50-state survey.<\/a> BMJ Ment Health. 2026;29(1):e302287<\/p>\n

34. Remmert JE, Guzman G, Mavandadi S, Oslin D. Racial disparities in prescription of antidepressants among U.S. veterans referred to behavioral health care.<\/a> Psychiatr Serv. 2022;73(9):984-990.<\/p>\n

35. Harman JS, Edlund MJ, Fortney JC, et al. The influence of comorbid chronic medical conditions on the adequacy of depression care for older Americans.<\/a> J Am Geriatr Soc. 2005;53(12):2178-2183.<\/p>\n

36. Olfson M, Blanco C, Marcus SC. Treatment of adult depression in the United States.<\/a> JAMA Intern Med. 2016;176(10):1482-1491.<\/p>\n

37. Remes O, Mendes JF, Templeton P. Biological, psychological, and social determinants of depression: a review of recent literature.<\/a> Brain Sci. 2021;11(12):1633.<\/p>\n

38. Mintz D. Combining drug therapy and psychotherapy for depression.<\/a> Psychiatric Times. 2006;23(11).<\/p>\n

39. Pies RW, Henssler JF. Antidepressant withdrawal syndromes: listening to the patient and taking it slow.<\/a> Psychiatric Times. 2026;43(2).<\/p>\n

40. Fava GA, Benasi G, Lucente M, et al. Withdrawal symptoms after serotonin-noradrenaline reuptake inhibitor discontinuation: systematic review.<\/a> Psychother Psychosom. 2018;87(4):195-203.<\/p>\n

41. Henssler J, Heinz A, Brandt L, Bschor T. Antidepressant withdrawal and rebound phenomena.<\/a> Dtsch Arztebl Int. 2019;116(20):355-361.<\/p>\n

42. Davies J, Read J. A systematic review into the incidence, severity and duration of antidepressant withdrawal effects: are guidelines evidence-based?<\/a> Addict Behave. 2018;97:111-121.<\/p>\n

43. Henssler J, Schmidt Y, Schmidt U, et al. Incidence of antidepressant discontinuation symptoms: a systematic review and meta-analysis.<\/a> Lancet Psychiatry. 2024;11(7):526-535.<\/p>\n

44. Volkmann C, Abulikemu S, Berwian IM, et al. Do withdrawal symptoms predict depression relapse after antidepressant cessation?<\/a> Eur Arch Psychiatry Clin Neurosci. 2026;276(2):749-760.<\/p>\n

45. Horowitz M, Taylor D. Tapering of SSRI treatment to mitigate withdrawal symptoms.<\/a> Lancet Psychiatry. 2019;6(6):538-546.<\/p>\n

46. Shapiro B, Cohrs D. Fluoxetine substitution for deprescribing antidepressants: a technical approach.<\/a> J Psychiatry Neurosci. 2025;50(4):E202-E209.<\/p>\n

47. Goldberg JF, McIntyre RS, Swartz HA, et al; American Society of Clinical Psychopharmacology Task Force on the Deprescribing of Psychotropic Medications. Recommendations for the deprescribing of psychotropic medications: a consensus statement from the American Society of Clinical Psychopharmacology Task Force.<\/a> JAMA Netw Open. 2026;9(2):e260043.<\/p>\n

48. Ghaemi SN. Symptomatic versus disease-modifying effects of psychiatric drugs.<\/a> Acta Psychiatr Scand. 2022;146(3):251-257.<\/p>\n

49. El-Mallakh RS, Briscoe B. Studies of long-term use of antidepressants: how should the data from them be interpreted?<\/a> CNS Drugs. 2012;26(2):97-109.<\/p>\n

50. Keller MB, Trivedi MH, Thase ME, et al. The Prevention of Recurrent Episodes of Depression with Venlafaxine for Two Years (PREVENT) study: outcomes from the 2-year and combined maintenance phases.<\/a> J Clin Psychiatry. 2007;68(8):1246-1256.<\/p>\n

51. Lam RW, Kennedy SH, Adams C, et al. Canadian Network for Mood and Anxiety Treatments (CANMAT) 2023 Update on Clinical Guidelines for Management of Major Depressive Disorder in Adults.<\/a> Can J Psychiatry. 2024;69(9):641-687.<\/p>\n","protected":false},"excerpt":{"rendered":"In the past year, American psychiatry has been in the spotlight\u2014though perhaps \u201cin the hot seat\u201d would be…\n","protected":false},"author":2,"featured_media":739932,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[60],"tags":[97,259,260],"class_list":["post-739931","post","type-post","status-publish","format-standard","has-post-thumbnail","category-mental-health","tag-health","tag-mental-health","tag-mentalhealth"],"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/posts\/739931","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/comments?post=739931"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/posts\/739931\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/media\/739932"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/media?parent=739931"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/categories?post=739931"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/us\/wp-json\/wp\/v2\/tags?post=739931"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}